Author + information
- Received October 12, 2019
- Revision received December 13, 2019
- Accepted December 13, 2019
- Published online March 2, 2020.
- aCell Signalling Research Group, School of Life Sciences, University of Nottingham, Nottingham, United Kingdom
- bCharité–Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany
- cDZHK (German Centre for Cardiovascular Research), partner site, Berlin, Germany
- ↵∗Address for correspondence:
Dr. Georgios Kararigas, Forschungshaus 2, Charite University Hospital, Hessische Str. 3–4, 10115 Berlin, Germany.
• HFpEF is a condition predominantly of postmenopausal women.
• Menopause-related E2 decline might contribute to HFpEF onset.
• E2 regulates several pathways involved in the pathogenesis of HFpEF.
• Targets for the prevention and therapy of HFpEF are necessary.
Heart failure (HF) is a complex condition affecting >40 million people worldwide. It is defined by failure of the heart to pump (HF with reduced ejection fraction) or by the failure of the heart to relax, resulting in reduced filling but with preserved ejection fraction (HFpEF). HFpEF affects approximately 50% of patients with HF, most of whom are women. Given that the annual mortality ranges from 10% to 30% and as there are no treatments specifically directed for HFpEF, there is a need for better understanding of the underlying mechanisms of this condition. We put forward the hypothesis that the decline of estrogen at menopause might contribute to the pathogenesis of HFpEF and we highlight potential underlying mechanisms of estrogen action, which may attenuate the development of HFpEF. We also discuss areas in which additional research is needed to develop new approaches for prevention and treatment of HFpEF.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received October 12, 2019.
- Revision received December 13, 2019.
- Accepted December 13, 2019.
- 2020 American College of Cardiology Foundation
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